DIP2A (Disco-Interacting Protein 2 Homolog A) is a type I receptor molecule with roles in cellular signaling, cardiovascular protection, and synaptic function . Anti-DIP2A antibodies are specialized immunological tools designed to detect and study this protein in research and diagnostic settings. These antibodies are critical for understanding DIP2A’s structural and functional roles, including its interaction with follistatin-like 1 (FSTL1) and cortactin, as well as its involvement in neurodevelopmental disorders like autism .
DIP2A antibodies are employed in diverse experimental workflows:
FSTL1 Interaction: DIP2A antibodies confirmed its role as a receptor for FSTL1, mediating cardiovascular protection via Akt signaling .
Synaptic Function: In Dip2a-deficient mice, antibodies revealed defects in dendritic spine morphogenesis and cortactin acetylation, linking DIP2A to autism-like behaviors .
Tissue Expression: Broad expression in neuronal, vascular, and reproductive tissues, validated via LacZ reporter mice .
DIP2A antibodies demonstrated its role as a receptor for FSTL1, a secreted protein that promotes endothelial cell survival and migration . Knockdown experiments using siRNA and anti-DIP2A antibodies showed reduced FSTL1 binding, Akt phosphorylation, and apoptosis resistance in hypoxic cardiac myocytes .
In Dip2a-knockout mice, antibodies revealed:
Spine Morphogenesis: Increased stubby spines and reduced mushroom-like spines in basal dendrites.
Synaptic Deficits: Thinner postsynaptic densities (PSDs) and impaired cortactin acetylation.
Behavioral Phenotypes: Excessive repetitive behaviors and social deficits, resembling autism spectrum disorder (ASD) .
LacZ reporter mice confirmed DIP2A expression in: